scholarly journals Expression pattern of neuronal and skeletal muscle voltage-gated Na+channels in the developing mouse heart

2005 ◽  
Vol 564 (3) ◽  
pp. 683-696 ◽  
Author(s):  
Volker Haufe ◽  
Juan A. Camacho ◽  
Robert Dumaine ◽  
Bernd Günther ◽  
Christian Bollensdorff ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Expression Pattern ◽  
Mouse Heart ◽  
Na Channels ◽  
Voltage Gated

Mechanism of modulation of the voltage-gated skeletal and cardiac muscle sodium channels by fatty acids

1997 ◽  
Vol 272 (2) ◽  
pp. C592-C600 ◽  
Author(s):  
S. Bendahhou ◽  
T. R. Cummins ◽  
W. S. Agnew
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Arachidonic Acid ◽  
Unsaturated Fatty Acids ◽  
Inactivation Kinetics ◽  
Na Channel ◽  
Na Channels ◽  
Channel Conductance ◽  
Na Current ◽  
Voltage Gated

Voltage-gated rat skeletal muscle and cardiac Na+ channels are modulated by exogenous unsaturated fatty acids. Application of 1-10 microM arachidonic or oleic acids reversibly depressed Na+ channel conductance and shifted the inactivation curve to hyperpolarizing potentials. These effects were not prevented by inhibitors of lipoxygenase, cyclooxygenase, cytochrome P-450 epoxygenase, or protein kinase C. Neither palmitic acid nor methyl ester oleate had an effect on the inward Na+ current, suggesting that trivial variations in membrane fluidity are not responsible for the Na+ current depression or kinetic changes. Arachidonic acid altered fast Na+ inactivation without changing the slow inactivation kinetics. Moreover, skeletal muscle Na+ channel gating currents were markedly decreased by 2 microM arachidonic acid. Finally, nonstationary noise analysis indicated that both the number of channels and the open probability were slightly decreased without change in the single-channel conductance. These data suggest that unsaturated fatty acids such as arachidonic and oleic acids 1) specifically regulate voltage-gated Na+ channels and 2) interact directly with Na+ channels, perhaps at a fatty acid binding domain, by decreasing the total gating charge and altering fast-inactivation kinetics.

scholarly journals Relationships between resting conductances, excitability, and t-system ionic homeostasis in skeletal muscle

2011 ◽  
Vol 138 (1) ◽  
pp. 95-116 ◽  
Author(s):  
James A. Fraser ◽  
Christopher L.-H. Huang ◽  
Thomas H. Pedersen
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Conduction Velocity ◽  
Electrical Response ◽  
Quantitative Description ◽  
Ion Concentration ◽  
Ionic Homeostasis ◽  
Voltage Gated ◽  
Concentration Changes ◽  
T System

Activation of skeletal muscle fibers requires rapid sarcolemmal action potential (AP) conduction to ensure uniform excitation along the fiber length, as well as successful tubular excitation to initiate excitation–contraction coupling. In our companion paper in this issue, Pedersen et al. (2011. J. Gen. Physiol. doi:10.1085/jgp.201010510) quantify, for subthreshold stimuli, the influence upon both surface conduction velocity and tubular (t)-system excitation of the large changes in resting membrane conductance (GM) that occur during repetitive AP firing. The present work extends the analysis by developing a multi-compartment modification of the charge–difference model of Fraser and Huang to provide a quantitative description of the conduction velocity of actively propagated APs; the influence of voltage-gated ion channels within the t-system; the influence of t-system APs on ionic homeostasis within the t-system; the influence of t-system ion concentration changes on membrane potentials; and the influence of Phase I and Phase II GM changes on these relationships. Passive conduction properties of the novel model agreed with established linear circuit analysis and previous experimental results, while key simulations of AP firing were tested against focused experimental microelectrode measurements of membrane potential. This study thereby first quantified the effects of the t-system luminal resistance and voltage-gated Na+ channel density on surface AP propagation and the resultant electrical response of the t-system. Second, it demonstrated the influence of GM changes during repetitive AP firing upon surface and t-system excitability. Third, it showed that significant K+ accumulation occurs within the t-system during repetitive AP firing and produces a baseline depolarization of the surface membrane potential. Finally, it indicated that GM changes during repetitive AP firing significantly influence both t-system K+ accumulation and its influence on the resting membrane potential. Thus, the present study emerges with a quantitative description of the changes in membrane potential, excitability, and t-system ionic homeostasis that occur during repetitive AP firing in skeletal muscle.

Sign in / Sign up

Export Citation Format

Share Document